Re: My Dad's neuropathy...

x-no-archive: yes

marcia wrote:

Really? Oh, that gives me great hope, Susan.

:-) :-) :-)


My dad has been so
depressed by his condition, and there was nothing I could do other than
sympathize with him. I've learned more from the great responses of
people on this thread than I have in a month of internet research. (It
seems the really important information is hidden away
somewhere...although I do now have two new websites to investigate).

How much Alpha Lipoic acid do you take? Is it more than the recommended
amount, or is the normal dose sufficient? I will make sure he starts
checking post-prandial blood sugar.

I can't believe his doctor apparently never told him any of this!


I took 600 mg time released to reverse the residual numbness of PNs in 3 mos. Over a year ago I had a bad relapse after bad holiday eating, and got rid of the pain in one week with low carbing and 1200 mg per day time released.

Here's some Medline research (some studies refer to it by its other name, thioctic acid):

J Neurochem 2003 Jun;85 Suppl 2:15



Therapy with antioxidants in human diabetic neuropathy.

Ziegler D
Deutsches Diabetes-Forschungsinstitut an der Heinrich-Heine-Universitat, Auf'm
Hennekamp 65, 40225 Dusseldorf, Germany, dan.ziegler@xxxxxxxxxxxxxxxxxxxxxxx

[Medline record in process]


Increased oxidative stress has been implicated in the pathogenesis of diabetic
polyneuropathy (DPN). Antioxidant treatment with alpha-lipoic acid (ALA) has
been shown to prevent or ameliorate experimental diabetic neuropathy, providing
the rationale for treatment in humans. A recent meta-analysis including four
controlled clinical trials provided evidence that treatment with ALA (600
mg/day i.v.) over 3 weeks is safe and significantly improves both neuropathic
symptoms and deficits to a clinically meaningful degree in patients with
symptomatic DPN. Moreover, oral treatment for 4-7 months tends to ameliorate
neuropathic deficits and cardiac autonomic neuropathy. Clinical and
postmarketing surveillance studies have revealed a highly favorable safety
profile of this drug. Based on these findings, a pivotal long-term multicenter
trial of oral treatment with ALA (NATHAN 1 Study) is under way aimed at slowing
the progression of DPN.

PMID: 12752990, UI: 22638617

1: Exp Clin Endocrinol Diabetes 1999;107(7):421-30 Related Articles, Books,
LinkOut


Alpha-lipoic acid in the treatment of diabetic polyneuropathy in Germany:
current evidence from clinical trials.

Ziegler D, Reljanovic M, Mehnert H, Gries FA.

Diabetes-Forschungsinstitut an der Heinrich-Heine-Universitat, Dusseldorf,
Germany. dan.ziegler@xxxxxxxxxxxxxxxxxxxxxx

Diabetic neuropathy represents a major health problem, as it is responsible for
substantial morbidity, increased mortality, and impaired quality of life.
Near-normoglycaemia is now generally accepted as the primary approach to
prevention of diabetic neuropathy, but is not achievable in a considerable
number of patients. In the past two decades several medical treatments that
exert their effects despite hyperglycaemia have been derived from the
experimental pathogenetic concepts of diabetic neuropathy. Such compounds have
been designed to improve or slow the progression of the neuropathic process and
are being evaluated in clinical trials, but with the exception of alpha-lipoic
acid (thioctic acid) which is available in Germany, none of these drugs is
currently available in clinical practice. Here we review the current evidence
from the clinical trials that assessed the therapeutic efficacy and safety of
thioctic acid in diabetic polyneuropathy. Thus far, 15 clinical trials have
been completed using different study designs, durations of treatment, doses,
sample sizes, and patient populations. Within this variety of clinical trials,
those with beneficial effects of thioctic acid on either neuropathic symptoms
and deficits due to polyneuropathy or reduced heart rate variability resulting
from cardiac autonomic neuropathy used doses of at least 600 mg per day. The
following conclusions can be drawn from the recent controlled clinical trials.
1.) Short-term treatment for 3 weeks using 600 mg of thioctic acid i.v. per day
appears to reduce the chief symptoms of diabetic polyneuropathy. A 3-week pilot
study of 1800 mg per day given orally indicates that the therapeutic effect may
be independent of the route of administration, but this needs to be confirmed
in a larger sample size. 2.) The effect on symptoms is accompanied by an
improvement of neuropathic deficits. 3.) Oral treatment for 4-7 months tends to
reduce neuropathic deficits and improves cardiac autonomic neuropathy. 4.)
Preliminary data over 2 years indicate possible long-term improvement in motor
and sensory nerve conduction in the lower limbs. 5.) Clinical and postmarketing
surveillance studies have revealed a highly favourable safety profile of the
drug. Based on these findings, a pivotal long-term multicenter trial of oral
treatment with thioctic acid (NATHAN I Study) is being conducted in North
America and Europe aimed at slowing the progression of diabetic polyneuropathy
using a clinically meaningful and reliable primary outcome measure that
combines clinical and neurophysiological assessment.

Publication Types:
Review
Review, Tutorial

PMID: 10595592 [PubMed - indexed for MEDLINE]

Metabolism 1999 Apr;48(4):504-10



Lipoic acid acutely induces hypoglycemia in fasting nondiabetic and diabetic rats.

Khamaisi M, Rudich A, Potashnik R, Tritschler HJ, Gutman A, Bashan N
Department of Clinical Biochemistry, Faculty of Health Sciences, Soroka Medical Center and Ben-Gurion University of the Negev, Beer-Sheva, Israel.

Lipoic acid (LA) is a unique antioxidant that increases peripheral glucose utilization in diabetic patients. This study was conducted to investigate whether the inhibition of glucose production could be an additional mechanism for the action of LA. Intravenous (i.v.) LA injection (100 or 60 mg/kg body weight) to fasting nondiabetic or streptozotocin (STZ)-induced diabetic rats caused a rapid reduction in blood glucose with no effect on circulating insulin levels. In vivo conversion of fructose to glucose was not inhibited by LA, whereas the gluconeogenesis flux from alanine was completely prevented. Reduced liver pyruvate carboxylase (PC) activity in vivo is suggested by the finding that LA induced a decrease in liver coenzyme A (CoA) content (44% and 28% reduction in nondiabetic and diabetic rats, respectively, compared with vehicle-treated animals) and liver acetyl CoA content (80% and 67% reduction in nondiabetic and diabetic rats, respectively). A reduction in plasma free carnitine (42% and 22% in nondiabetic and diabetic rats, respectively) was observed in LA-treated animals, and acylcarnitine levels were increased twofold. This could be attributed to elevated levels of C16 and C18 acylcarnitine, without a detectable accumulation of lipoylcarnitine. Under such conditions, a significant increase in the plasma free fatty acid (FFA) concentration (204% in nondiabetic and 151% in diabetic animals) with no elevation in beta-hydroxybutyrate levels was noted. In conclusion, this study suggests that short-term administration of LA at high dosage to normal and diabetic rats causes an inhibition of gluconeogenesis secondary to an interference with hepatic fatty acid oxidation. This may render LA an antihyperglycemic agent for the treatment of diabetic subjects, who display glucose overproduction as a major metabolic abnormality.

PMID: 10206446, UI: 99221287

Free Radic Biol Med 1999 Aug;27(3-4):309-14



Oral administration of RAC-alpha-lipoic acid modulates insulin sensitivity in patients with type-2 diabetes mellitus: a placebo-controlled pilot trial.

Jacob S, Ruus P, Hermann R, Tritschler HJ, Maerker E, Renn W, Augustin HJ, Dietze GJ, Rett K
Hypertension and Diabetes Research Unit, Max Grundig Clinic, Buhl and City Hospital, Baden-Baden, Germany. snjacob@xxxxxxxxxxxxxxxxxxxx

Alpha-lipoic acid (ALA), a naturally occuring compound and a radical scavenger was shown to enhance glucose transport and utilization in different experimental and animal models. Clinical studies described an increase of insulin sensitivity after acute and short-term (10 d) parenteral administration of ALA. The effects of a 4-week oral treatment with alpha-lipoic acid were evaluated in a placebo-controlled, multicenter pilot study to determine see whether oral treatment also improves insulin sensitivity. Seventy-four patients with type-2 diabetes were randomized to either placebo (n = 19); or active treatment in various doses of 600 mg once daily (n = 19), twice daily (1200 mg; n = 18), or thrice daily (1800 mg; n = 18) alpha-lipoic acid. An isoglycemic glucose-clamp was done on days 0 (pre) and 29 (post). In this explorative study, analysis was done according to the number of subjects showing an improvement of insulin sensitivity after treatment. Furthermore, the effects of active vs. placebo treatment on insulin sensitivity was compared. All four groups were comparable and had a similar degree of hyperglycemia and insulin sensitivity at baseline. When compared to placebo, significantly more subjects had an increase in insulin-stimulated glucose disposal (MCR) after ALA treatment in each group. As there was no dose effect seen in the three different alpha-lipoic acid groups, all subjects receiving ALA were combined in the "active" group and then compared to placebo. This revealed significantly different changes in MCR after treatment (+27% vs. placebo; p < .01). This placebo-controlled explorative study confirms previous observations of an increase of insulin sensitivity in type-2 diabetes after acute and chronic intravenous administration of ALA. The results suggest that oral administration of alpha-lipoic acid can improve insulin sensitivity in patients with type-2 diabetes. The encouraging findings of this pilot trial need to be substantiated by further investigations.

Publication Types:


Clinical trial
Multicenter study
Randomized controlled trial
PMID: 10468203, UI: 99396279

Diabetes 1997 Sep;46 Suppl 2:S62-6



Alpha-lipoic acid in the treatment of diabetic peripheral and cardiac autonomic neuropathy.

Ziegler D, Gries FA
Diabetes Research Institute at the Heinrich Heine University, Dusseldorf, Germany.

Antioxidant treatment has been shown to prevent nerve dysfunction in experimental diabetes, providing a rationale for a potential therapeutic value in diabetic patients. The effects of the antioxidant alpha-lipoic acid (thioctic acid) were studied in two multicenter, randomized, double-blind placebo-controlled trials. In the Alpha-Lipoic Acid in Diabetic Neuropathy Study, 328 patients with NIDDM and symptomatic peripheral neuropathy were randomly assigned to treatment with intravenous infusion of alpha-lipoic acid using three doses (ALA 1,200 mg; 600 mg; 100 mg) or placebo (PLAC) over 3 weeks. The total symptom score (TSS) (pain, burning, paresthesia, and numbness) in the feet decreased significantly from baseline to day 19 in ALA 1,200 and ALA 600 vs. PLAC. Each of the four individual symptom scores was significantly lower in ALA 600 than in PLAC after 19 days (all P < 0.05). The total scale of the Hamburg Pain Adjective List (HPAL) was significantly reduced in ALA 1,200 and ALA 600 compared with PLAC after 19 days (both P < 0.05). In the Deutsche Kardiale Autonome Neuropathie Studie, patients with NIDDM and cardiac autonomic neuropathy diagnosed by reduced heart rate variability were randomly assigned to treatment with a daily oral dose of 800 mg alpha-lipoic acid (ALA) (n = 39) or placebo (n = 34) for 4 months. Two out of four parameters of heart rate variability at rest were significantly improved in ALA compared with placebo. A trend toward a favorable effect of ALA was noted for the remaining two indexes. In both studies, no significant adverse events were observed. In conclusion, intravenous treatment with alpha-lipoic acid (600 mg/day) over 3 weeks is safe and effective in reducing symptoms of diabetic peripheral neuropathy, and oral treatment with 800 mg/day for 4 months may improve cardiac autonomic dysfunction in NIDDM.

Publication Types:


Clinical trial
Multicenter study
Randomized controlled trial
Review
Review, academic
PMID: 9285502, UI: 97429864

Susan
.

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